I am interested in the role of protein kinase C in neuronal plasticity.
Initially we were able to report changes in the distribution of this
critical enzyme within the hippocampus during classical conditioning
and other forms of learning in rabbit, rat and the marine snail, Hermissenda.
More recently, myself and Dr. JV Sanchez-Andres have been pursuing studies
on the distributional changes in PKC as assessed by quantitative
autoradiography,
within the neonatal rabbit hippocampus. In addition to the quantitative
autoradiography studies, we have also been studying the
electrophysiology
of neonatal CA1 pyramidal cells.
What follows is information that we are abstracting to the Society for
Neuroscience for the November 1991 meetings:
CA1 cells recorded from littermates showed a characteristic pattern,
consisting of A) adaptation, associated with B) firing a small number
of spikes (1-3) when a depolarizing pulse was applied. By Day 15
post partum, all cells showed the adult pattern consisting of a
moderate
adaptation which slowed down the spiking frequency along a depolarizing
pulse. The change of pattern was associated temporally with the day
in which the Neonates opened the eyes (NEO).
The pattern of PKC distribution seen before NEO was qualitatively
different
from that seen either after that point in developement or in adults.
This was manifested by extremely dense bands of 3H-phorbol ester
binding
on either side of the stratum pyramidale both in CA1 and in CA3. These
bands dramatically delineated the cell body layer and were localized to
the most proximate apical and basilar dendritic zones. After NEO, this
pattern shifted to one reminiscent of that seen in an adult classically
conditioned animal 24 h into retention (i.e stratum oriens and
pyramidale
showing together the greatest binding; Olds et al. Science 1989).
We are interested in what other members of the neuroscience community
make of these results. We are especially interested in possible
interpretations
of the activated PKC as zones of *inactivated* potassium channels.
Finally we would be very interested in the theoretical implications
of such phenomena in the hippocampus during this critical developmental
period.
--
************************************************************************
*****
* James L. Olds Ph.D. Laboratory of Cellular and Molecular
Neurobiology*
* domain:olds at helix.nih.gov NINDS, NIH, Bethesda, MD. 20892
USA *
************************************************************************
*****